Wednesday, July 20, 2011

Weight Gain and Weight Loss in a Traditional African Society

The Massas is an ethnic group in Northern Cameroon that subsists mostly on plain sorghum loaves and porridge, along with a small amount of milk, fish and vegetables (1, 2). They have a peculiar tradition called Guru Walla that is only undertaken by men (2, 1):

This social institution, aimed at prestige acquisition, includes a massive overfeeding representing twice or threefold the habitual daily intake.

It lasts two months, during which they are overfed on sorghum, milk, fish and vegetables (mostly sorghum, but with an increased ration of milk as well). They eat beyond the point of nausea, day and night, and expend as little energy as possible. Calorie intake exceeds 8,000 kcal per day. According to two detailed studies of nine Massas, by the end of Guru Walla, they had gained about 37 pounds (17 kg), mostly as fat* (2, 3).

What happened after they stopped overeating? When they returned to their typical diet, which contains 75% carbohydrate, 11% fat, and 15% protein, the investigators found something interesting (3):

Rapid and substantial decreases in body weight and fat were observed in all subjects during the first 3.5 mo after the cessation of overfeeding. Subsequently, a more progressive decrease was noted up to the last measurement session. Thirty months after the end of Guru, the group had lost all of the overfeeding-induced weight gain.

This supports two ideas that may be starting to sound familiar:

Body fat mass is regulated in both directions (i.e., both increases and decreases are opposed)**. This is supported by numerous overfeeding and underfeeding studies in both humans and rodents.

Plain, repetitive starchy foods do not lead to fat gain and can support fat loss.

* This is less fat gain than expected due to the energy intake, suggesting "substantial thermogenesis" in response to the overfeeding. Their bodies appeared to have mounted a compensatory response aimed at countering fat gain.

** According to this hypothesis, obesity represents an increase in the "setpoint" around which fat mass in regulated. This Guru Walla study is especially interesting because it looks at body fat regulation in a non-industrial society, which should have well functioning homeostasis mechanisms that have not been damaged by industrial living. As fatness is prized in this society, they had no incentive to deliberately lose fat after Guru Walla.

139 comments:

According to the one abstract they engaged in 61-65 days of 'fattening'. Trying hard not to expend energy, I'm assuming their energy expenditure was roughly 2500 calories a day. So they were eating an excess of 5500 calories per day. By my calculations, if all of that had of been stored as fat they would have gained roughly 100 pounds. Subtract the 37 pounds they did gain and we're left with 63 pounds they managed to burn off - roughly 3500 calories a day. That is an impressive - almost unbelievable - amount of thermogenesis.

Do you think the same amount of thermogenesis would have occured had they been overeating more on bland, monotonous forms of fat?

And do you think the palatability of the starch effects thermogenesis? Would pasta and fresh bread be burned off as readily as sorghum?

Hi Stephan, do you know if the milk was fermented or not? This is relevant because if it wasn't, then the milk was laden with lactose, which is a very sweet taste for anyone who doesn't have sugar or fruit in their diet.

Without salt on the fish or vegetables, I can imagine they would have been fairly bland too. Maybe fat mass setpoint was raised by the sweetness of the milk. I'd like to know just how much milk they got during the fattening period.

They gained weight force-feeding themselves to the point of nausea. On this bland, monotonous diet it required heroic efforts to gain weight and still they only managed to store a little over a third of their excess calories as fat. That is a lot different than the insidious weight gain you see in industrialized societies where people merely eat until they are satisfied. And unlike these people, people in industrialized societies have great difficulty losing weight on modern diet regimens once they become obese.

Stephan is not recommending that people stuff themselves with bland food to the point of physical pain.

I think what he meant is that they lost the weight eating to appetite on a bland, primarily starch-based diet. That is very consistent with his recent ideas about food reward.

What I'm wondering is why on Earth are they doing that? Is there some evolutionary explanation?

OK, maybe there is some status gained by being bigger and heavier, I don't know what could be the origin of that, but - in this case - why would they then lose all that weight? Why come back to the "lower" status?

If you read the article, you'll see that they compensated for any vomiting by taking the vomited meal out of the equation. You'll also see that they measured energy content of stool to estimate how much energy that was just passing through- Actually, the daily consumption of energy was about 6700 kcal (28,2 Mj) after adjusting for fecal losses.

About two months ago, whenever it was you started this series, I tried a low-flavor diet. I lost appetite and weight rapidly at first, then weight loss slowed and stopped. Then I became ravenously hungry and gained it all back plus more. In other words, exactly the same as any other diet.

All the overfeeding experiments I've seen are always done in males. This is probably useful to other males but it needs to be pointed out that the results are NOT relevant for females whose bodies seem optimized to hold onto that fat for obvious evolutionary reasons.

Yes, it's a huge amount of thermogenesis. Thermogenesis with overfeeding is higher with carbohydrate. They likely would have gained more fat had they been overfed with fat.

Hi Gunther,

I don't know.

Hi Brock,

I don't know the details of what you did, but here's my impression from your comment. You tried a low-flavor diet and it caused weight loss. You became hungry, went off the low-flavor diet, then gained fat back. Is that correct?

It sounds to me like it worked, but you just weren't able to maintain it. If you were hungry, it's because you simply weren't eating enough. This plan is not about starvation, it's about eating simple foods to fullness.

If I recall, you've already lost a substantial amount of weight by eating a home-cooked whole food diet. So you were already most of the way there when you started the low-flavor diet. I never claimed this way of eating would turn an obese person into an Abercrombie model-- there is a portion of the excess fat mass that will likely be retained.

At this point, I've received a number of e-mails and comments from people who have tried the method. They are nearly all positive, including two people who have broken through weight loss plateaus they had reached on a low-carb diet.

Hi Jenny,

Women did not evolve to be obese any more than men did. I think that post-menopausal women have more trouble maintaining weight due to the loss of estrogen however.

Stephan, you wrote before that the short-term effect of dopamine is anti-obesogenic, the reason chronic consumption of rewarding food is obesogenic is because of eventual desensitization actually leading to lower dopamine signaling, is that correct?

Then it seems to me that a diet that intermittently spikes dopamine yet allows you to remain sensitive to it, would be better than a bland-food-all-the-time diet.

This lines up with my personal experience as all the naturally lean people I know do regularly enjoy highly rewarding food, they just don't eat it all the time. I'm guessing this would be one positive feaure of intermittent fasting too, as the long period without food allows you to restore dopamine sensitivity, while the hearty meal you then get to enjoy during the eating window will give you a big spike in dopamine.

Colldén, a link inside that reference says that the fattening period lasts three months. In Stephan's example, the excess feeding lasts two months.

In both cases, these subjects were probably still insulin-responsive. It is not surprising that after the excessive caloric intake, they eventually returned to a normal weight. They had not been subjected to the intrauterine environment of a pre-diabetic mother. They had not spent their whole young lives eating sucrose, HFCS and snacks made of refined carbohydrates. They were not returned to such a diet after the overfeeding experience. This is an interesting cultural practice, but I am not sure it applies to people who are experiencing obesity in the United States, particularly insulin-resistant people who are experiencing such obesity.

This goes back to dietary toxicity. The food reward mechanism plays a "damaging" role when it comes to highly rewarding toxic foods, however, if the diet is free of toxicity the body's homeostatic mechanisms are quite powerful.

Colldén, I understand that you were replying to Jenny's point. However, the article you linked provides an excellent additional example suggesting that a few months of overfeeding in a population that is probably still insulin-responsive, does not produce long-term obesity in men or in women.

I don't understand what insulin sensitivity has to do with it. Weight loss does not seem to depend on the degree of insulin sensitivity if I understand correctly. Furthermore, high-carbohydrate diets based on whole foods improve insulin sensitivity:

I agree that high-carbohydrate diets based on whole foods may improve insulin sensitivity, but this may have something to do with glycemic index rather than with carbohydrate percentage. Here is a meta-analysis:

Thanks for the references, I'll have to think about it. The first one is definitely suggestive of different responses in people of different insulin sensitivity, however it does not establish whether insulin resistance, or something else that correlates with insulin resistance, determines the effect. Also, everyone lost weight on the low-fat diet regardless of insulin sensitivity, it's just that those with better sensitivity lost more.

The last paper you provided was in diabetics-- it makes sense to me that a low glycemic index diet could be somewhat helpful for glycemic control in diabetics, but the same does not appear to be true in non-diabetics. Long-term controlled trials show no differences in food intake, body weight or insulin from following a low-GI diet as compared with a high-GI diet. If anything, the trend is for high GI to improve insulin sensitivity.

I thought I would just leave a quick note to say how this is an interesting and well-presented blog. Keep up the good work and I look forward to reading more posts in the future. I also found a very interesting and a great blogsite that gives interesting tips about beauty and nutrition at http://www.beravishing.com/

The actual number of pounds gained isn't at all heroic, it's just thermodynamics. No one is debating that forcing bland calories into your body beyond your calorie needs will result in a certain level of fat gain. Once it enters our bodies, energy is energy regardless of how well it tasted going in.

It is interesting, as I noted in a prior comment, that their bodies burned nearly two thirds of those excess calories as body heat. I'm not so sure that would have happened had they been gorging on doritoes and haagen daaz. But that's not what is important anyways.

As I said, Stephan isn't recommending we force-feed ourselves to the point of self-torture.

What matters is how our ad libitum relationship with the diet effects our health.

On this particular diet, they had to force-feed themselves to the point of nausea only to store a little over a third of those excess calories as fat. Their bodies were aggressively trying to remain lean through thermogenesis throughout the over-feeding. Then when they return to ad-libitum eating, every pound falls off. In other words, they lose every pound eating as much as they want. No calorie counting, no cutting carbs, no ravenous hunger, no slowing down of the metabolism and subsequent rebound weight gain.

I thought I had read the article fully and carefully, as painful as that is given Taubes' mind-numbing prose.

Allow me to borrow directly from the post itself:

"Second, let’s say you’re carrying around 40 pounds of excess fat and you put on that 40 pounds over the course of 20 years, as many of us do. When you’re in your late 20s, say, you’re still lean, and then, lo and behold, you celebrate your fiftieth birthday and you’re obese and your doctor is lecturing you on eating less and getting to the gym regularly (and probably writing you a prescription for Lipitor, as well). Now, if you gain 40 pounds of fat over 20 years, that’s an average of two pounds of excess fat accumulation every year. Since a pound of fat is roughly equal to 3500 calories, this means you accumulate roughly 7000 calories worth of fat every year. Divide that 7000 by 365 and you get the number of calories of fat you stored each day and never burned – roughly 19 calories. Let’s round up to 20 calories, so we have a nice round number. (In the new book I discuss this issue in a chapter called “The Significance of Twenty Calories a Day.”)

So now the question: if all you have to do to become obese is store 20 extra calories each day on average in your fat tissue — 20 calories that you don’t mobilize and burn — what does overeating have to do with it? And why aren’t we all fat? Twenty calories, after all, is a bite or two of food, a swallow or two of soda or fruit juice or milk or beer. It is an absolutely trivial amount of overeating that the body then chooses, for reasons we’ll have to discuss at some point, not to expend, but to store as fat instead."

And somehow you take issue with these words of mine:

"Gary Taubes wrote a blog post illustrating that the typical weight gain experienced in our society is due to an excess of a mere 20 calories daily over a number of years."

Taubes shows that a 40 pound weight gain over 20 years amounts to a mere 20 calories a day being stored as fat. Obviously it's different for each individual. And certain people may gain 40 pounds in one year, and none the next. All I am borrowing from Taubes is the fact that many of us gain weight due to small amounts of fat being placed into storage gradually over many years.

I'm not debating his opinion on why that happens. Well I'm not at the moment anyways.

Perhaps you should read what I said a little more carefully, or fully for the first time.

I will say, in retropsect, that my reasoning was misleading. If a person were to consume 8000 calories a day from junk food, they would still likely see a significant rise in thermogenesis. However, I do suspect it would be a lot less.

I don't see this as evidence that body mass is regulated against obesity, any more than a ball falling to the ground is evidence that physical forces are at work which regulate mass so that solid objects stay on the ground. Gravity does not regulate the placement of balls on the ground; the ball ending up on the ground is merely is the result when all physical factors affecting the position of an object are accounted for. The ball stays on the ground once dropped because there are not more forces acting on it than gravity. If a sufficiently strong wind were to occur, the ball would then move from its placement on the ground.

Similarly, this group of humans does not fatten and remain overweight because they do not have the disease of obesity - that "force" is not acting on them. All it indicates is that this group of human beings does not posses the genetics/was not exposed to the predisposing factors which lead to metabolic diseases, therefore they are incapable of becoming hyperinsulinemic and significantly obese. They must force feed themselves to gain fat (meaning to say they are nauseated and their body is like "plz dont eat") and once they stop the force feeding, the weight is lost. The body resists obesity because the body does not have this disease.

The fact most people do not grow tumors on their skin does not suggest there is a regulating force keeping your skin at this "set point" of cell mass. The fact that some people DO grow tumors on their skin only suggests that there is a process going on in that person's body which is resulting ins kin cell hyperplasia. It does not suggest that the balance of skin cells have a "set point" that your body is constantly defending against increases in skin cells. I mean if you want to be extremely logical then yes, there is a system preventing excessive skin cell growth (if you research development cancer and tumors, a tumorous or cancerous cell is very different and it no longer monitors adjacent cells which regulate growth of the cells). However, when discussions cancer and tumors, it is useless to point that out because the problem is not a "loss of set point" as pertaining to skin cell balance, the problem is this disease, this pathology where certain cells in the body keep multiplying and multiplying with no regard what so ever for function.

It is important to conceptualize a tumor this way, because the problem is not a loss of something (a "set point" accounting system) but a gain of something abnormal (rapidly growing cells with abnormal genes fetal genes turned on).

Obesity is precisely like this. The person is obese not because they have lost their defense against obesity - In an extremely logical way, this statement is true, but from a pathophysiological standpoint, this loss of set point is merely secondary to the primary problem which is fat tissue that is abnormally expanding due to abnormal endocrine environment, which in turn is secondary to abnormal genetics/mitochondrial function.

Conclusion 2 is irrational, because the group of humans studied did not have the disease of obesity, so it is totally invalid to draw any conclusions about any form of obesity from this group of obesity resistant human beings.

It would be like making the argument that phenylalanine merely promotes higher levels of dopamine and norepinehprine in a random sample of negative PKU humans; therefore, a low phenylalanine diet is of no utility and has no role in the disease of PKU.

Stephan, about super-stimuli, so you think video games are harmful? What about other potentially addictive-like activities like intense music, movie-series watching, certain fiction reading (harry potter) or role-playing (dungeons and dragons) or other kinds of games? I've seen people spend hour after hour in such activities, often at the expense of other more productive, healthful things (like sports, studying, etc.), and react with severe anger or distress when such activities are denied, just as may happen with tv and video games. Are they super stimuli? Personally, I can't avoid feeling somewhat sad, and confused, since, besides the fact that I think video-games can be art, I have a strong emotional connections to many I played in my youth (just as one can have one with a movie or book), and is one of the things I love to do the most... And yes, it often takes quite a bit of my time.

Also, I remember Ryan Koch talking about this same issue in a african tribe, but with women. Gotta search the link.

You didn't misquote Taubes, and you didn't misunderstand - you just took him out of context.

He was using that equation to show that there is no way that such slight adjustments in individual eating behavior on a day to day basis could lead to obesity. It is not as easy as refusing one slice of bread (or less) per day to prevent weight gain - calories in/calories out is affected by other physiological mechanisms.

He wasn't saying that 20kcal/day is how weight gain occurs; he was using this obviously ridiculous idea to show that there is something else at work.

He illustrated that a 40 pound weight gain over 20 years equates to roughly 20 calories of fat having been stored per day. I never once mentioned Taubes outlook on why we gain weight, simply used this statement of his to illustrate that we typically put on weight very slowly over the years due to our bodies storing slight daily excesses.

This overfeeding experiment made me think of Taubes '20 calories a day' concept.

From Taubes' statement:

"It is an absolutely trivial amount of overeating that the body then chooses, for reasons we’ll have to discuss at some point, not to expend, but to store as fat instead"

I'm not defending the calories in/calories out hypothesis.I'm saying something causes our bodies to store small amounts of fat gradually until our weight threatens our health. And once we become obese we have an extremely difficult time losing the weight.

These tribesman ate 8000 calories a day and burned a large share of that as body heat. Then the moment they resume their typical eating habits the weight sheds off.

I was only using Taubes statement to mark the contrast between them and us.

Stephan wrote: "At this point, I've received a number of e-mails and comments from people who have tried the method. They are nearly all positive, including two people who have broken through weight loss plateaus they had reached on a low-carb diet."

I would be curious whether these people are now also more likely to postpone eating until they are hungry. Did any of them mention anything like that, such as in no longer eating snacks and such?

I see too that the Egecioglu et al. (2011) article you cited earlier in support of this food reward theory mentions ghrelin (the hunger hormone) as a possible mediator for the effect, in that ghrelin increases the reward value of food. But this is perhaps opposite to the way I (with my admittedly limited background in physiology) would tend to look at it. Hopefully this isn't too far out to lunch:

ASSUMING that ghrelin levels are more strongly elevated in the case of homeostatic ("true") hunger than hedonic (eating for pleasure) hunger, and assuming that one is less likely to experience homeostatic hunger in an environment surrounded by hedonically rewarding foods (food you are constantly nibbling on), then a bland food environment (with nothing tasty to nibble on), should result in increased levels of ghrelin (whether chronically or intermittently). Ghrelin, I believe, also helps drive activity levels, especially pre-meal food-anticipatory activity (which I get big time when I intermittently fast), which makes sense in that if you're hungry, it is adaptive to become more active so that you will go out and forage for food. This in turn means that in an environment in which one is frequently experiencing homeostatic (true) hunger, there will be a tendency for ingested calories to be channeled into activity rather than fat. Conversely, in an environment in which one rarely experiences homeostatic hunger - because you are surrounded by foods that entice you to eat when you are not truly hungry - there will be a tendency to channel calories into fat rather than activity. Thus, set point for body weight should be relatively higher in a rich food environment (as though your body is saying“I’m never truly hungry; must be lots of food easily available; best for me to begin storing fat for the future”) than in a bland food environment (“I’m still sometimes hungry; food procurement could still be an issue; I better channel some of these calories into activity and keeping fit”).

I notice that the authors of that article mention that “common levels of obesity are associated with low circulating levels of ghrelin”, which is a problem for their theory, but they speculate that “brain ghrelin” could nevertheless be high. But the theory proposed here is more parsimonious in that it doesn’t require any such speculation; obese individuals should have low levels of both circulating ghrelin and brain ghrelin.

If ghrelin, or something like it, is involved in the food reward effect in something like the way I’ve described, then we also don’t have to worry about such issues as how much one enjoys a truffle when satiated versus a slice of bread when famished. The critical is not the taste of food per se, but rather the extent to which certain kinds of food motivate eating even when one is not homeostatically hungry, thereby reducing overall levels of ghrelin.

As Taubes illustrates, while simply eating to appetite our diet causes our bodies to horde a miniscule daily average of fat until obesity and all its deadly comorbid conditions develop. We then starve ourselves on our diet and have immense difficulty losing the weight. Our bodies struggle to be fat.

These people eat painfully beyond appetite on their diet and their bodies struggle to waste shocking amounts of excess calories as body heat. Then eating to appetite afterwards, with no starvation response, their bodies shed every pound gained. Their bodies struggle to be lean.

I'm very interested why the latter diet allows for what is obviously a much healthier relationship with food.

I believe Stephan is arguing that the key difference is the lower food reward in their diet. I agree.

You think I'm somehow arguing that haphazardly overeating 20 calories a day caused the obesity epidemic, as though we were somehow in control of that 20 calories. I'm not saying that whatsoever.

There is this silly divide between the "calories in/calories out" hypothesis and the "failed regulatory mechanism" hypothesis.

Both are true. It's just a simple fact that we became fat because more calories came in than out. And a failure of the regulatory mechanisms that should be keeping our weight in check is the reason why that happened.

I like Stephan's ideas on food reward because it explains how that failure takes place in a very sensible way.

I believe as he does that industrial food has been engineered to be so palatable that it has an almost drug like effect. The psychological gratification causes our bodies to ingest more of this food than we need until we become obese. Basically, the effect is so powerful the mind no longer cares what it does to the body. The same thing is seen in various other addictions. Our bodies don't want lung cancer, yet we become addicted to cigarettes. Our bodies don't want cirrhosis of the liver, yet we become addicted to alcohol.

Gary Taubes wrote a blog post illustrating that the typical weight gain experienced in our society is due to an excess of a mere 20 calories daily over a number of years.

Maybe you didn't mean to mention Taubes' outlook, but that little "due to" in there will surely confuse anyone (not living inside your head) into thinking that you think that Taubes thinks weight gain is due to an excess of 20 calories a day over a number of years. Now that I know that you don't think that I will start thinking about other things to think about. Glad we cleared that up.

@evgeny In traditional societies obesity is a sign of wealth and status, as wealthy people are exposed to the triggering factors for obesity (prenatal hyperinsulinemia + chronic excess of available carbohydrate & fat calories, etc).

These people gorge on calories for the same reasons people in america starve themselves and boast of being a size 0. In their culture, that body type is a sign of wealth and status. In our culture, an emaciated figure is a sign of wealth and status , as our population is afflicted with obesity and the poorest people are most likely to be obese, due to generation after generation of people exposed to prenatal high insulin and high leptin levels from an energy rich high carbohydrate diet, which is shown in scientific studies to lead to deterioration of normal glucose tolerance and obesity as an adult. Every generation is fatter than the last largely because our body weight and glucose tolerance has already been programmed before we even enter the world. If your mother is an obese diabetic, you will be an earlier on set and fatter diabetic than she was, on and on. Diabetic obese toddlers happen today for this reason.

They go back to the lower status body type probably because they know it cannot be maintained indefinitely because as peasants they are relatively glucose tolerant and obesity resistant... the same reason americans starve for vacations and celebrations then they return to their heavier figure during every day life. Very few people in our culture lose weight and keep it off, for the same reason these obesity resistant people find they cannot gain weight and keep it on.

I would expect this to happen. Temporary weight loss due to temporary appetite reduction. No change in weight status long term. Flavorful food does not cause obesity, any more than oxygen rich oxygen tanks cause COPD. People with the disease may be observed to eat more and crave more but that's an expected result of their disorder, similar to how someone with COPD can't walk very well without their oxygen tank, and screams for a nasal cannula after taking a few steps.

@JennyGood point, women are far more vulnerable to developing obesity due to the independent effects of estrogen/progesterone vs testosterone.

However I think in this specific population... it has less to do with gender and more to do with the fac these people were not exposed to the prenatal / postnatal factors that actually cause obesity. Obesity resistant females when put in overfeeding studies are shown to behave like obesity resistant males - they vomit, they feel disgusted of the food, they lose the weight they gained after the overfeeding stops. Assuming of course she is an obesity resistant female.

Gender only seems to be another factor that predisposes how fat one gets and how easily one fattens. If you look at any group of humans rife with obesity (e.g. your typical low income neighborhood) the females are always far far more obese than the males in general and this is the effect of progesterone/estrogen when combined with other causative factors for obesity. Estrogen and progesterone, like carbohydrate, is just another triggering/exacerbating factor but does not cause the problem itself. Female gender just affects how fat you get and how easily your obesity is decompensated/triggered.

Speaking as a female and in the high progesterone phase of menstural cycle right now I can personally attest that progesterone definitely decompensates metabolic control, profoundly augments appetite and specifically encourages body fat gain/hyperinsulinemia. This is fairly well shown and the most egregious of the female reproductive hormones is progesterone. "PMS" with fatigue and ravenous hunger and foul mood is a direct result of progesterone. Birth control methods which are progestserone based are always associated with severe PMS symptoms like acne, depression, massive weight gain/obesity triggering and blood sugar disorders. On the other hand the low/no progesterone birth control methods (estrogen based ones) are relatively good for mood, acne, and are far less likely to cause weight problems.

IT's amazing so much myths are written on the web about female endocrine system, most women are lead to believe that estrogen does what progesterone does and vice versa. All the progesterone cream sheisters out there have women believing that progesterone leads to weight loss and fights depression and gives energy. HA! If you actuqally read the testimony of women taking HRT they pretty unanimously confirm that progesterone supplementation is fatiguing, depressive and tends to augment appetite/lead to weight gain.

http://joe.endocrinology-journals.org/content/106/2/225.abstractIn contrast, progesterone implants in normal and diabetic rats increased body weight gain, adiposity, insulin receptor concentration and both basal and insulin-stimulated rates of lipogenesis in adipose tissue, again without affecting insulin sensitivity. Progesterone did not affect serum insulin concentrations in normal or diabetic rats but accelerated the decline in serum glucose concentrations which occurred during an overnight fast in diabetic rats.

Basically, progesterone makes you into a fat storing machine and this is why women eat more during PMS, and may partly account for the progressive weight gain that seems to afflict females, with major increases in fatness seen after each child birth (pregnancy involves progesterone levels which are extremely high, much higher than the 2 week increases of progesterone seen every cycle - pregnancy disastrous for an obesity prone person).

Men may prefer thinner women with small waists specifically because thinness is a marker for nulligravida status. It's quite obvious why men would prefer young females who are less likely to have ever been pregnant. Evolution does not reward men who are cuckolded.

Women , due to progesterone, tend to trigger /significantly exacerbate obesity after pregnancies. Similarly, thinner women tend to look younger / youthful specifically because younger females who have not had much progesterone exposure, and no pregnancies, are therefore not heavy with body fat.

I am always mistaken for being younger than my age and I do think the only reason people think I am younger is because it is very rare for a nearly 29 year old to have my body type. My body type, however, is quite common for women in their early 20s or late teens, and I tend to think the progressive effects of progesterone exposure and prengancies are reasons why.

I can't help but observe all the women I know seemed to have become significantly and permanently fatter after prengancies... I am thin, and I have never been pregnant, and most females I know who have never been pregnant are also relatively thin compared to the women I know who have had children.

@Roberto - The point of this illustration on behalf of Taubes is to make it obvious how bizarre, absurd and unlikely is the assumption that people get fat because they eat too many calories.

20 calories a day for 20 years? Really? That doesn't sound unlikely to you? That doesn't make you think "gee, it must be something else, how can an error of accounting THIS SMALL result in such a profound shift in body mass? It must be something else, it must be a purposeful effect of the body to gain body fat... such a tiny insignificant amount of chewing gum every day, clearly the body is driven to fatten and it is not an accident."

That's what Taubes wants you to think when he says "20 calories per day for 20 years leads to obesity". I find it scary that some people read this and agree with him literally - they find it reasonable to conclude that yes, obesity is caused by eating too many calories because after all, 20 calories for 20 years.

"Do you think if you fed an obese person this same massas diet, that they would have the same metabolic/endocrine profile as a massas person?

Or do you think it is more likely that the obese person would gain far more weight on the bread and milk gorging, and fail to lose it after the overfeeding experiment?"

Stephan commented earlier that he has had positive feedback from people following a diet based on reduced food reward. As he said, some even broke through plateaus they had reached on low carb diets. So that partially answers your question.

From what I gather, your supposed panacea for obesity is a low-carb diet coupled with leptin injections. I seriously doubt that is a solution for obesity in all people. In either case, leptin therapy is not accesible for the vast majority of people. And the past 40 years, sinced Atkins popularized the low-carb diet, has shown that a lot of people have little to no weight loss on low-carb dieting and often have their health suffer as as a result of it. So where do people turn?

Having read your various monologues I seriously doubt you've even found a healthy solution for your own obesity. Even if you have maintained your weight loss - which those close to have apparently described as anorectic - you've clearly been on a roller coaster ride. You've reported mood swings, hair loss, fluctuations in your weight, fatigue, and the periods of energy you do describe sound almost manic.

What is your response to the countless people who have given their own anecdotal reports of complete failure on low-carb diets?

@Roberto"He illustrated that a 40 pound weight gain over 20 years equates to roughly 20 calories of fat having been stored per day. I never once mentioned Taubes outlook on why we gain weight, simply used this statement of his to illustrate that we typically put on weight very slowly over the years due to our bodies storing slight daily excesses. "

No. You keep restating this, but taubes specifically made that proposition to point out how ridiculous it is to assume that "slight daily excesses" lead to obesity. This is the exact opposite of Taubes argument, and the fact you think his example is a good one for supporting the "gradual overeating" hypotehsis of obesity is very concerning. The example neither supports Taubes views (which you puport not to care about or agree with),a nd it is also a very bad example to support the idea that gradual over eating leads to obesity. In fact, it clearly shows that such a trivial, insignificant amount of eating when averaged out over time accounts for major accumulation of body fat depots speficially is evidence against over eating being the cause of obesity. We all know that thin people do not consciously count their calories every day... animals don't, dogs don't, cats dont, no human does except humans who already have the disease of obesity. Given that no human alive is aware of the calorie content of their food, and given that such tiny small minuscule amounts of energy averaged out over the years can account for a massive 40 pounds of body fat excess, it strongly suggests that food intake merely facilitates obesity but does not cause it.

"That doesn't make you think "gee, it must be something else, how can an error of accounting THIS SMALL result in such a profound shift in body mass?"

'Bert' and 'alexi de sadesky' asked me the exact same thing, and I explained to them why I do not thing haphazardly consuming an excess of 20 calories a day causes obesity. Please, scroll back and find the several responses I gave to land on the same page with them.

Me:

He illustrated that a 40 pound weight gain over 20 years equates to roughly 20 calories of fat having been stored per day. I never once mentioned Taubes outlook on why we gain weight, simply used this statement of his to illustrate that we typically put on weight very slowly over the years due to our bodies storing slight daily excesses.

This overfeeding experiment made me think of Taubes '20 calories a day' concept.

From Taubes' statement:

"It is an absolutely trivial amount of overeating that the body then chooses, for reasons we’ll have to discuss at some point, not to expend, but to store as fat instead"

I'm not defending the calories in/calories out hypothesis.I'm saying something causes our bodies to store small amounts of fat gradually until our weight threatens our health. And once we become obese we have an extremely difficult time losing the weight.

These tribesman ate 8000 calories a day and burned a large share of that as body heat. Then the moment they resume their typical eating habits the weight sheds off.

I was only using Taubes statement to mark the contrast between them and us.

I DON'T THINK that gradual over-eating in of itself leads to obesity. I stated in as many ways as I could conjure that I think a failure of our regulatory body mass regulation system often leads our bodies to store small amounts of calories gradually until we become obese.

I was contrasting our situation with that of these tribesman:

As Taubes illustrates, while simply eating to appetite our diet causes our bodies to horde a miniscule daily average of fat until obesity and all its deadly comorbid conditions develop. We then starve ourselves on our diet and have immense difficulty losing the weight. Our bodies struggle to be fat.

These people eat painfully beyond appetite on their diet and their bodies struggle to waste shocking amounts of excess calories as body heat. Then eating to appetite afterwards, with no starvation response, their bodies shed every pound gained. Their bodies struggle to be lean.

Stephan may have had some positive reports from a few isolated people, but it is impossible to draw any evidence about the efficacy of a low reward/palatability diet based on this. For all we know the letters were totally fabricated, or they were from people like brock who are experiencing a very temporary appetite redeuction (until metabolic/endocrine dynamics predominate).

When someone says they found a new great diet... wait a few weeks and then ask how they are doing.

I do not think my prescription is a solution for all forms of obesity, but I do think it will be effective for most forms of obesity, as most forms of obesity seem to clearly be mediated by hyperinsulinemia (and hyperinsulinemia then logically translates into a REQUIREMENT for levels of leptin to be replaced after weight loss, due to sensitizing fat cells to multiply, which reduces the amount of leptin each fat cell will make given an equal fat mass between people).I say that most forms of obesity seem to be mediated by hyperinsulinemia as most obese humans eat a diet which is clearly insulinogenic. Fast food and sugar and such things and high calories. IT seems as if the development of their obesity is a direct result of chronic and prolonged hyperinsulinemia due to aquired, and/or genetic loss of normal glucose processing and normal insulin processing. The diet merely triggers.

The leptin is only important after the obesity correction. The insulin is important only to terminate the obesity progression, and to reverse the fat cell hypertrohpy.

Handle both sides and you have a naturally thin person who used to be obese.No it won't work for all obese people. If you have a rare form of obesity - MCR4 mutation, leptin receptor mutation, congential leptin deficiency, severe extreme hyperinsulinemia due to abnoramlly functioning insulin receptors, that does not respond to dietary glucose restriction, damage to hypothalamus, etc etc etc... no this won't work at all for you.But most fat people today do not have these specific, extreme abnormalities. Most fat people today are chronically overproducing insulin because our glucose tolerance is relatively poor due to prenatal / postanatal factors, genetics, and we are also eating a very high carbohydrate diet as well, and an extremely micronutrient poor diet. Lack of chromium and inositol and magnesium alone may not account for much but together, they can seriously impair how insulin works in your body... and combined with such massive dietary glucose loads it is safe to say you will use up your reserves of glucose tolerance factors very quickly (and they are not being replaced because your calories come from pizza and ramen).

Taubes was stating clearly that many people gradually - slowly - gain weight until they become obese. He quite literally meant that in a lot of people it equates to only 20 calories a day being stored.

Taubes:

"It is an absolutely trivial amount of overeating that the body then chooses, for reasons we’ll have to discuss at some point, not to expend, but to store as fat instead."

The basic message of his post is that this doesn't happen by accident due to gradual overeating (gluttony). I agree with him. I don't think it has a single thing to do with carbs spiking insulin however.

I do admit a period after weight loss where I had a mild eating disorder, but I am by far from an anoretic. Merely because I am thin and am weary of shit food does not make me anoretic. Just got done eating a massive plate of mussels with butter sauce, a piece of garlic butter bread, and a big hamburger with cheese and a few fries.

I admit I do have a mood disorder, there have been times I have had extreme depression and there have been times I have had manic energy. I fail to see what this has to do with this argument at all. It would be like me saying "your points are invalid because you are fucking BALD and you clearly can't cure your baldness can you so what do you have to say about this discussion."

Having a mood disorder - which by the way became EXTREMELY BETTER when I controlled my glucose processing problems, I was torporously depressed prior to that - does not mean that I have nothing to say.

My moods have not gotten worse for doing this, they have gotten far far far better and I have such nothing depression compared to the monstrous burden I started with.

And keep in mind, Stephans food-reward ideas aren't geared solely toward the obese, but also to those who would like to avoid becoming obese. And do you honestly think metabolically healthy people need to avoid blueberries, brown rice and sweet potatoes on a low-carb diet to avoid obesity?

"Stephan may have had some positive reports from a few isolated people, but it is impossible to draw any evidence about the efficacy of a low reward/palatability diet based on this. For all we know the letters were totally fabricated, or they were from people like brock who are experiencing a very temporary appetite redeuction (until metabolic/endocrine dynamics predominate)."

I have yet to see a single reference backing any of your facts and the sole justification for your recommendations is your own n=1 experience.

Woo, you present very strong arguments. My first thought when I read this post was "are these Massas insulin resistant or insulin sensitive"? This study has no probative value in the realm of this "food reward" discussion. It does not support or refute it. Actually, it only seems to support that the body has a very efficient pathway to deal with excess calories when insulin sensitive, which is not controversial at all. *head scratch*

Good points. My understanding is that hedonic hunger and "true homeostatic hunger" (which i will call gut hunger) are actually seperate and completely disconnected systems.

People often say that after eating big meals, they "always" have space for desert, something sweet. i.e., thier hedonic hunger was not satiated.

In my own case, I can eat alot of chocolate, candy, bread, rice, potato foods etc, but shortly after the grumbling in my stomach will return and I will have a strong taste for meat foods. So in this case my gut hunger was not satiated.

Stephan, thanks for considering the impact of insulin resistance on responsiveness to various diets. In the first two journal articles I linked, the participants were free-living but were provided with food, and it is possible that they complied with the protocol. If they did, that may explain why the insulin resistant patients lost some weight on the low-fat diet.

I mention this because it is hard for a person without insulin resistance to understand the drive to eat that is produced by insulin resistance. The consistently-high levels of insulin make it difficult for the body to go into lipolysis. The insulin-resistant body prefers to use glucose as an energy source and produces enough true hunger that a person who has access to food will eventually reach for a carb-filled snack to obtain some relief. It is possible to overcome these urges with willpower, but in most cases the willpower eventually flags and the person returns to frequent carb feeding, elevated blood insulin, and ongoing resistance to lipolysis. Again, thanks for considering this perspective, Stephan.

I second Woo's question (though not the implication) about what do you think would happen if an obese American went through a Massa fattening. Would they, like the Massa guys, get a little fatter and then return to their original level of fat? Would they get quite a bit fatter and just keep going, due to a "broken" metabolism? Might they even end up at a lower weight, as Matt Stone might predict, the overfeeding having had positive effects on reward/setpoint systems?

I don't think video games are inherently harmful, nor do I think high-reward food is inherently harmful. It depends on the dose, the frequency and individual susceptibility. If you can play video games twice a week for an hour each, then I don't see any problem. If you feel compelled to play for four hours a day at the expense of other activities (e.g., sleeping), then I'd say it's time for some soul searching.

Some people can smoke one cigarette a day for their entire lives, never become addicted and never suffer any real health consequences. Others smoke one cigarette a day, become addicted, start smoking a pack a day and end up wheezing for 20 years and dying of lung cancer. I think you just have to be honest with yourself about what kind of personality you have and how strongly you're drawn to the habit.

There have been a number of overfeeding studies in humans, some of which included overweight participants. They have not found any difference in the ability of overweight vs lean individuals to defend their current level of fat mass. That said, I'm not aware of any overfeeding studies that involved obese people. However, obese people clearly have an elevated "setpoint", as they will initiate a homeostatic response when their body fat and leptin levels are still well above those of a lean person.

I don't know exactly what would happen to an obese person on the Massas overfeeding regimen, besides the fact that they would gain fat. I suspect they would lose the excess fat they had gained during overfeeding after the overfeeding stopped. However, I'm pretty sure if you put the average American obese person on the typical (non-overfeeding) Massas diet, they would lose fat.

'Plain, repetitive starchy foods do not lead to to fat gain and can support fat loss.'

In the early 1970's I lived in Vietnam for 14 months and observed many traditional Vietnamese meals. It was always the same: rice and vegetables with a little fish, and still less meat. (Sometimes a little fruit was consumed but not as much as you would have thought for a tropical climate.)

Of course there was a war going on but these people were definitely not starving. They ate perfectly normal amounts of food per meal. And unsurprisingly, not one of the aforementioned was appeared remotely overweight. Look at pictures from the period. Ask people who were there. One will remain thin on such a diet.

For various reasons I adopted the same basic diet (not as a mimic but as an anti-heart disease measure) for nearly 30 years and I, for better or worse, remained thin exactly like the Vietnamese did. At 55 my EBT calcium score was zero.

I have moved on to far more fats in my diet for a number of reasons, Stephen's larger point is sound.

Most of the people who have contacted me didn't specify the level. Most simply ate plain home-cooked food with no added fats, salt, spices.

I only know of one person who is trying level 5. The jury is still out on whether it will work for her-- she had already lost a considerable amount of weight prior to trying it so that is a situation that has a lower likelihood of success.

I think insulin has something to do with appetite - but I've not found studies that decouple the role of insulin from leptin. If leptin resistance forms first before insulin resistance I could imagine a neuro learning of a regulatory response that could change the set-point. (It could take some years to unlearn such a response - during that time one would have to avoid eating things that raise tryg or contain lectins )

Peri-menopausal women in industrial societies are usually estrogen dominant. That is, estrogen levels are too high relative to progesterone levels.

This is most often due to anovulation. The bulk of progesterone is produced by the corpus luteum in the ovary after ovulation.

I consider problems with ovulation & hormone levels another DOC.

PMS, menstrual migraines and other cycle related problems are most often caused by a disturbance in progesterone levels during the luteal phase. Most often, progesterone levels are not high enough, or fall too quickly too early in the cycle. Progesterone levels can also be too high.

Xenoestrogens in the environment also contribute to estrogen levels which are too high relative to progesterone levels.

Hormones, estrogen or progesterone, added to cosmetics and not disclosed on the label is another big problem. Watch out for those age defying lotions and foundations.

You need enough progesterone to balance estrogen. Neither one is "good" and neither one is "bad".

Most women approaching menopause find themselves in a situation where progesterone levels are declining ahead of estrogen levels. The problem, in general, is NOT "too little estrogen".

After menopause, either estrogen and/or progesterone levels may be too low, but again, still, it's more common for progesterone levels to be too low relative to estrogen.

It's also important to remember that progesterone increases the sensitivity of estrogen receptors, and visa versa. Adding progesterone in supplement form may make matters worse in the short term as the P increases the sensitivity of the E receptors and a woman really feels the estrogen dominance.

http://www.johnleemd.com/store/premenstrual_syndrome.html

The progestin used in birth control pills is NOT the same as bioidentical progesterone. Progesterone is natural to the human body, and progestin is not. They are two entirely different things, and we should be careful not to substitute "progesterone" for "progestin".

http://www.virginiahopkinstestkits.com/everywomanbc.html

The commonly repeated belief that menstrual problems are simply due to low estrogen and that post-menopausal problems are simply due to low estrogen is dangerous.

Another complication is the common use of serum for measuring sex hormones. You've got to measure what's in the tissues (saliva) and not what is bound up and floating around in the bloodstream (serum). Apples and oranges.

@Peter MSo basically you are a non-obese person who has never had obesity and never developed obesity, presumably you are not genetically at risk for obesity either (e.g. fat/diabetic parents). Yet for some reason you assume that if people eat like you they can cure their existent obesity? Huh?

That would be like me saying "by eating rice3 + veggies every day I will ward of sickle cell anemia" meanwhile I don't have it, never had it, and have no genetic relatives with this disorder.

I don't think we are getting that obesity is real and it is genetic - enviroinment only predisposes/ triggers.

For example, I have PCOS. Not all glucose intolerant women get PCOS. To get PCOS you need a certain set of genetic traits:1) The thecal cells of the ovaries must be sensitive to insulin/LH, excessively so.2) There must be a weak genetic ability to synthesize d-chiro-inositol.3) Central dopaminergic insensitivity also helps develop PCOS/anovulation4) It also helps if you have hepatic enzymes which genetically are very sensitive to insulin mediated increases in cytocrhome P450 17 hydroxylase which synthesizes excessive amounts of 17-hydroxyprogesterone (which in turn becomes DHEA and testosterone). High levels of insulin upregulate the activity of this enzyme leading to adrenal gland mediated hyperandrogenism.

IF YOU ARE A FEMALE WHO IS GLUCOSE INTOLERANT AND HYPERINSULINEMIC, but you lack those above traits, you will NEVER develop PCOS no matter how fat you are or how high your insulin is.

On the other hand, if you are a female with each and every one, you may have very severe PCOS even upon mild glucose intolerance and mildly elevated insulin.

So, when you cite that you have failed to develop obesity thus far in your life... is it because of your diet, or is it because you are innately, genetically, obesity resistant and at BEST you can only gain a pound or two eating your absolute worst, much like my brother and thin family members?

The ARKO mouse lacks aromatase and so cannot make estrogen well. This is a very specific form of estrogen deficiency. Since cholesterol is the substrate from which estrogen is made, it is possible that feeding the ARKO mouse cholesterol bolsters its substrate and so helps increase the rate of estrogen conversion (to compensate for non-functional aromatase). This would not at all be relevant to estrogen deficiency by other causes and would only be relevant to estrogen deficiency due to sluggish aromatase.

Just a guess.

Either way I would not necessarily extrapolate effective treatments from an ARKO mouse to naturally estrogen low humans (e.g. menopausal females) because it is quite possible it is arko mouse specific.

@JinThat is the conventional progesterone cream sheister POV. You are reiterating the same bad advice given to women online and the goal seems to basically sell progesterone cream.PMS is almost entirely a syndrome of progesterone excess, not estrogen excess. Food craving, hunger, fatigue, acne and depression are direct 100% caused by progesterone.

THere are a few PMS symptoms caused by declining estrogen - headache/migraine is due to declining estrogen, some of the depression may also be from declining estrogen. Bloating is estrogen mediated but progesterone helps a lot too.IT is a complete and total myth that PMS is caused by low progesterone, and again, the goal is to sell progesterone cream.

Progesterone is definitely "bad" form a modern POV. It makes you sleepy, sluggish, working is difficult, it makes you clearly gain body fat, it lowers mood and energy. For a modern woman who is expected to go to work every single day even if she has high progesterone, and for a modern woman who wants to have a slender stylish figure, progesterone is not helpful. Unfortunately, you healthfully live without it either, but it's definitely a PITA. Women would not be as prone to obesity if progesterone did not so profoundly trigger it. There is a reason all women get - and stay - obese after childbirth, and why nulligravida women are slim with tiny waists but mothers look more and more like "memaws" the more children they have. Progesterone is that reason.I mean, if women were not expected to work 9-5 jobs and stay slim/energetic/youthful then yea, progesterone wouldn't be bad. It all depends on priorities I guess.Progesterone directly antagonizes estrogen receptors and causes them to downregulate, actually. Progesterone helps lower estrogen activity.

No one said menstrual problems were due to low estrogen. I said they were due to high progesterone.

Most menopausal symptoms are directly the result of estrogen deficiency,however. This really isn't up for debate it's almost proven.

I don't need to do more reading. I'm a female and observant and I don't believe dumb gurus. I know that when estrogen is surging at ovulation I feel fabulous and look great, and I can follow my malaise along a curve with the rise and fall of progesterone. Immediately after ovulation I "crash" which is due to a fall of estrogen and a small rise of progesterone. This crash is BRUTAL and I am ravenous, so fatigued I can barely move my body.I then recover and feel better on day 2 and 3.After day 3, when progesterone begins to rise from the corpus luteum, I gradually develop a MASSIVE INSATIABLE APPETITE and this lasts until about 2 days before menstruation. I also become so profoundly fatigued and numb and tired it's like I am dead. I feel like someone drugged me with tranqs. Working can be IMPOSSIBLE at this time. Today I stared at a medical chart for like 5 minutes not even moving. My energy is so abysmal. I barely even want to move. I do, however, want to continuously eat. I am eating a TON of food and have gained visible fat.The symptoms are peak 7 days after ovulation which matches the peak of progesterone.

2 days before menstruation, typically, my appetite drops, my mood improves, my energy picks up, and I feel good again. I may have manic symptoms at this time but not always (I have observed progesterone withdrawal is a manic trigger due to blocking estrogen and increasing GABA in the brain, like an antiepileptic).

I don't buy that "natural progesterone" bullcrap. I have never taken BCP and my natural progesterone is pretty awful, thx.Iknow it's progesterone because I only ever feel this way when progesterone is high and you can correlate my crappiness to the curve of progesterone secretion.I know it is NOT estrogen because I feel my very best the week before ovulation when estrogen levels are climbing. This is all rather typical for many women. Women eat less and feel best the week of ovulation.

What I was hoping to communicate is simply this: an entire society (the Vietnamese, 1970s) was living on an abundance of rice and vegetables as the bulk of their calories, and yet virtually none of these people became overweight. Perhaps I should not have mentioned that circumstantially I ate very similarly for many years afterward and remained thin. So, I am not advocating for the diet, or using myself as some perfect example, just passing along, what was observably true for that society, at that time.

You believe that estrogen deficiency may be responsible for weight gain in post-menopausal women. I don't buy it! I am a PM woman who does not take HRT, didn't buy into the BS and propaganda of the pharmaceutical industry during the intense marketing of conventional HRT in the 90's nor the bio-identical hormone sales pitch of 2000 +. I am leaner now and in better cardiovascular health than during my estrogen years. Why because I move my body! Women need to be physical at all ages and many women over 50 won't walk around the block. Moreover, in any basic biology text, you will read that estrogen can contribute to fat storage. After puperty females get more curves and it isn't about lean muscle mass! I find the medicalization of menopause to be really offensive. It is not a disease; it is is a natural part of a female's life. Lastly, I suspect but would not claim to "believe" that insulin resistance and other health issues might result from years of consuming an american diet high in sugar, processed foods, HF cornsyrup and heat-damaged omega 6 oils. All of the which might be part of the weight gain problem in older woman.

What I see in these fattening or overfeeding observations is one consistency: participants lost the weight they gained AFTER going back to their normal diet.

So basically, they didn't lose the weight by continuing to overfeed. I believe this is key because it means that overfeeding itself will not necessarily lead to fat loss, unless perhaps other tactics that will discourage hunger (such as a simpler, less rewarding diet as you have suggested, Stephan).

This is why these subjects and also the ones in the Keys study were able to drop the pounds after they returned to their normal diet: their normal diet/lifestyle was not conducive to maintaining the excess weight. In our current society, this may be difficult to duplicate without implementing specific restrictions to encourage appetite regulation.

Is there any reason to favor low reward food other than for weight control?

DOC track w/obesity, correct? And according to Taubes there are mechanisms associated with (processed?) carb intake that lead to weight gain AND DOC, therefore skinny folks like me should still be careful.

You have not stated outright that fat causes disease as Don Matz has....however, your recomendations by default favor a very low fat diet. You do have many older posts though that seem to exonerate fats in DOC and actually go further by implying that fats (esp dairy) may play a role in staying healthy (vitamin K, CLA, etc...).

Would those following a low reward approach miss out on benfits from full fat dairy or have you changed your mind on that? I have experimented with lower fat food because of some symptoms I was having while eating low carb Paleo. It is very difficult to keep fat as low as you (and Don) seem to be suggesting while still including full fat dairy in the diet....

By the way, on glucose/insulin and carbs:I can appreciate that spikes are normal and OK... I was still worried that fasting levels could be affected though and was a bit nervous about upping carbs for this reason.

Just got some blood results back and my fasting glucose went down to 75 (down from 85 w/low carb paleo which was down from 95 on high carb non-paleo). BUN was high hand CREAT low....

@bentlyj74 & @sandraIt is a fact many if not most women gain and retain body fat after pregnancy. The fact you did not, or the fact you went on a radically different diet after childbirth does not dispute the fact that progesterone causes body fat to grow. But, the question is.. .after childbirth is it AS EASY to lose weight and be thin as it was BEFORE childbirth? All women will unanimously agree it is much harder to lose weight after each child birth because the body is programmed to permanently defend a higher weight. That's not to say weight can't be lost, it is just way more difficult before progesterone mediated adipocyte hyperplasia .

I do not get classical PMS myself. I don't consider myself to have "PMS", rarely is my mood negative or agitated premenstrually. However, I almost always experience a significant increase in appetite (this was true even on leptin) and I also experience a significant decrease in physical energy and swiftness of thought.

There is nothing behavioral to attribute this to, it clearly ebbs and flows with the level of progesterone in my body. For example, last night I had a decrease in appetite and an increase in physical energy as well as mood. Today I have a low appetite and a lot of energy. I know this means that tomorrow or the next day I will get my period because the decrease in appetite and increase in energy/alertness/mood is a sure sign of progesterone declining. I have observed this over and over again. It is not psychological and there is hard scientific evidence to support the sedating, fattening nature of progesterone.

Peter -But the point I am making is that it is useless to prescribe diets for obese people , based on the eating habits of a group of humans who are obesity resistant by genetics.

As a RN, I work with many filipinos. Ethnically they are not so dissimilar to vietnamese, far more related than ethnic NAs, ethnic africans, or caucasians. There was a period of spanish rule in the Philippines but genetically they are most similar to asians.

I've observed filipinos are extremely obesity resistant. Even when they eat the same fattening food all americans eat, they CAN NOT gain much if any body fat and remain small and slim. Even when they have been here for generations eating this food, they still stay small. For the most part.They simply, genetically, rarely have the genes for obesity. So, are the vietnamese thin because they eat rice and veggies... or are they thin because they can not be obese even if they live in america and drink soda and eat potato chips, because their ethnicity has entirely lost the genes to detect and respond to seasonal trends of food availability due to an extensive history of agriculture?This is not surprising as they (east asians are from a culture which has a long tradition of agriculture and so would not have retained any seasonal fattening/hibernation genes. Obesity as I said before I believe is strongly related to hunter gatherer tendency to view an increase in carbohydrate as a sign of impending fall and winter, and so it triggers fat gain (as all animals do who prepare for the winter season, this is marked by a decrease in energy and an increase in body fat synthesis and appetite).You will find that human beings who are ethnically from cultures which are heavily agricultural are rarely predisposed to obesity. I believe the very high rates of obesity observed in america is due to the fact so many of us have metabolism genetics heralded from non-caucasian, non-asian hunter gatherers. We have many indiginous americans (e.g. mexicans, other latin americans, NAs), we have a large african population, and even our caucasian population is ethnically diverse and mixed with these other groups. Speaking personally I am "caucasian" but my tendency to obesity and PCOS was clearly inherited from my african grandmother, who lived in a tribe as recently as my great grandmother. I have green eyes and pale skin but I have my grandmother's genetics when it comes to processing glucose and responding to seasonal shifts. My "purely caucasian" grandparents were entirely obesity resistant and do not respond this way to a glucose based diet.

I have observed most obese americans are like me. Even if they are "white" they have recent ancestors who were inidigenous americans and this is where their vulnerability to obesity and glucose disorders comes from.

Native americans who are purely NA suffer the worst fate and are pretty much dead in the water on this agricultural diet.

Woo, not to be intentionally contrary but I see plenty of southeastern Asians living in the US who are overweight.

No one is suggesting, however, that glucose/insulin dysfunction does not contribute to a tendency to obesity in anyone regardless of ethnic background. But for the vast majority of those with normal glucose regulation a 'calorie appropriate' diet rich in safe starches does not equal inevitable weight gain. And it seems very hard to believe that any ethnic group is entirely 'obese resistant.' Individuals yes. Groups, no.

FWIW, I believe Stephan is saying something important that the so-called Paleo community might broaden their collective perspective on. What I'm NOT saying is that I think a starch heavy diet is necessarily optimal. Just don't blame carbohydrate by itself on all the ills of modern societal obesity. There are so many other forces at work here. People are being marketed to death (literally) by corporate interests. And those eating habits have essentially become entrenched in the culture.

(1) While your theory that pregnancy produces fattening is interesting, it can also be observed that childless women often gain weight and thicken at the waist as they age.

(2) Your theory about ethnic reasons for fattening is also interesting. But as an "n" of one, my family is pure white, traced back at least five generations, going back to Germany, England and Scotland (where I declined to pay the fees to pursue the records further). Yet we have a solid tendency to put on weight in response to carbohydrate. I wish that being Caucasian were a protection against obesity, but in my family's case, it's not.

Stephen-I don't know if this has been brought up yet (I haven't read all of the comments), but I found the article by Chris MasterJohn, "Is Insulin Resistance Really Making Us Fat?"(http://blog.cholesterol-and-health.com/2010/11/is-insulin-resistance-really-making-us.html), extremely fascinating. Although the highlighted study was done on mice, the link between leptin resistance and obesity was really driven home (as well as the lack of connection between insulin resistance and obesity-in fact, the insulin receptor knock out mice were a bit leaner than the controls). Since insulin resistance often tracks with leptin resistance, it's understandable that insulin has been made out to be the bad guy by so many. And since Leptin is a relatively newly discovered hormone, it's indeed understandable that the paradigm has not yet shifted (if it truly translates over to humans), at least among the blogging public.

Thomas, the problem with insulin receptor knockout mice is that the insulin receptor can only be knocked out in one tissue at a time, e.g., liver, brain, muscle, fat, beta cells, etc. (If there is a whole-body insulin receptor knockout, the animal dies shortly after birth.) The article you reference is talking about liver insulin receptor knockout mice. However, muscle-specific insulin receptor knockout mice had increased adipose tissue mass and hypertriglyceridemia, which are symptoms of the metabolic syndrome. (Joslin's Diabetes Mellitus, p. 161.) From the same source, neural-specific insulin receptor knockout mice were slightly hyperphagic and mildly obese.

Progesterone isn't going to cause me fatten any more than oxytocin is going to cause me to pass out face first in my soup and drown.

These are very exaggerated claims for mundane hormone fluctuation.

Prior to pregnancy I found it difficult/impossible to GAIN weight so I can't comment on difficulty losing it.

Was that due to hitting the genetic lottery or due to the 3 types of dance, swimming, and weight training I did for several hours on the average day on top of walking to and from wherever I was going to do something else then coming back to a home cooked low stimulus meal [Soda? Is it my birthday?] most often followed by a hot bath and an early bedtime.

There are so many variables in play there and I think they are all likely contributors to overall well being.

@stargazey-Chris mentions in the article that, at least in Rats, hepatic insulin resistance leads to systemic insulin resistance-so I was assuming that systemic insulin resistance was being considered. He also makes a pretty sweeping statement:

"...insulin resistance as it occurs in humans could, perhaps, cause leptin resistance. However, if it does not cause leptin resistance, it is very unlikely to make people fat."

He does not make the distinction between hepatic insulin resistance and that of muscle, nerve or fat in this statement, so I'd be interested to hear his comments (or Stephens) regarding your statement about the muscle and neural insulin receptor knockout mice.

In fact, human hepatic insulin resistance (insulin resistance of the liver) looks nothing like what happens in the hepatic insulin receptor knockout mice. The livers of these mice don't respond to insulin at all. In humans, this insulin resistance is "selective. The livers of "insulin resistant" humans continue to manufacture fat and send it out into the blood as triglycerides in response to insulin, but fail to suppress the production and export of glucose in response to insulin.

In humans, insulin resistance of the liver leads to increased triglycerides in the blood.

As described here, elevated triglycerides make it difficult for leptin to cross the blood-brain barrier producing leptin resistance. In starvation, an excess of triglycerides is adaptive and allows the person to delay satiation. In human hepatic insulin resistance, an excess of triglycerides also delays satiation, but with the effect of allowing the person to eat to excess.

@AlanYou're right technically the ground is a counter force resulting in no additional movement however my point stands. The point I was making is that physical laws when all accounted for are the only reason objects stay where they stay.

Body fat is the same. There is not "regulating force" keeping body fat exactly at some "set point weight", set point is merely short hand for the body weight one tends to settle at when all physiological "forces" acting on your fat mass are accounted for. It's not some magical immutable thing which some hormone is keeping set at a specific number. To an extent set point does exist... it is definitely true people have ranges of body weights they naturally fall when internal and external factors are accounted for. It's just not true that the body is "defending against obesity". Obesity is not being defended against any more than normally replicating & functioning cells "defend against cancer". An absence of cancer and a resistance to malignancy does not suggest there is an "anti cancer system" in the body. Cancer , when present, is the addition of something new, extra and abnormal.

Filipinos do get fat like every other human being, but the point I was making is that if you took a random sample of filipinos and compared them to a random sample of african americans, caucasians, or native americans, you would find the filipinos were relatively obesity resistant. NOTHING is absolute. Just like not all germans have the genetics for blue eyes, and not all swedes have blonde hair, it's also true not all filipinos remain thin and lean on a high carbohydrate diet. However when you scan a population sample of filipinos compared to latin americans or african americans you find they are way way smaller and far more obesity resistant.

I've never seen a 300 pound filipino for what it is worth. They tend to be very small in stature, small boned, and fail to accumulate significant body fat. I've seen plenty of chubby ones but never a significantly obese one... on the other hand, my african american and latin american and occasionally caucasian coworkers are significantly and extremely obese. Diets exactly the same.

I want to clarify that when I made the statement about ethnic differences and propensity to obesity I was not speaking in absolutes. There will be "purely caucasian" people who are prone to severe obesity and diabetes. There will be native amerians who do not develop obesity and diabetes.

Just like a population sample of germans will show not all have blue eyes, however the genetics for blue eyes are disproportionately represented among a sample of ethnic germans when compared to ethnic nigerians.

This ethnic difference is a very real reason why there are such profound differences in obesity rates in america compared to , say, japan.

Obesity is a genetic disease just like any other - whether or not you get it depends not only on your diet, but your genetics. The various traits predisposing to obesity are more or less prevalent among ethnic groups. To deny this is to deny reality. It's quite clear certain ethnic groups do better (or worse) on agriculture, carb diets and are more or less predisposed to obesity.

Yes, aging is a risk factor for fattening as well, but so is pregnancy. I suspect a young childless woman is thinner than an aginging childless woman is on average thinner than an aging mother. There is not ONE factor affecting weight. Aging and motherhood are independent factors and combined they exacerbate the trend to gain weight.

As bentley said, I agree with, progesterone does not CAUSE fattening, it's just a factor, just like the many many others that cumulate into developing obesity. When it comes to body fat, risk for obesity, and differences between men and women, the progesterone vs testosterone difference is the primary reason. Testosterone breaks down fat, raises dopamine, progesterone builds it up and causes sedation / suppression of the CNS.

I've observed, for example, while on supplemental leptin... progesterone would certainly make me hungrier but it would not lead to body fat gain.

However, now that I no longer take supplemental leptin and just rock my basal level, which is low, I find that the high progesterone points of the month correlate with pretty signifiant eating and clear body fat gain. The weight I have gained has been in spurts and it's been primarily during the 10 day progesterone high (2 days after ovo, 2 days before menses... that range of time = super hungry and tired).

When the progesterone begins to decline a bit, even slightly (e.g. yesterday my appetite dropped A LOT and today it is even lower) then I find the over eating totally stops and my energy gets normal and better.

Interesting bentley that you could not gain weight before pregnancy...but now presumably you can gain weight after pregnancy. Do you not see this as evidence that perhaps pregnancy helps the body to store fat and remain fat?

Women who are naturally predisposed to obesity for other reasons can be expected to have a more profound reaction to pregnancy and supraphysiological progesterone.

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@Wooo, thanks again for your clinical descriptions of how basic science works out in practice. I don't know about the rest of the commenters here, but as a Ph.D., I sometimes forget that what works in a dish of cells or in a genetically modified mouse, does not necessarily apply to a human being. You make me back up and look at the whole picture, and I need that.

@Thomas, you're welcome.

@Kathy, @lancy, @Vance, don't your sponsors realize that your ad-comments would be much more believable if you used standard American spelling and grammar? (Sorry, everybody. That's been bugging me for a while and I just had to say something.) /rant

James,Thanks, I must have missed that... Still Stephan points out that the Massas diet is about 11% fat. Perhaps I read between the lines incorrectly, but he seems to be suggesting VERY low fat= low reward = weight loss. Such a diet cannot include much whole milk, cheese and butter.

Wooo doesn't know what she is talking about re: pregnancy. Most women who start having kids when young have less fat gain than women who never have kids or start very late in life, all things being equal.

The delay on exercising fertility affects fat gain more than the exercising of the fertility.

We can find thousands of examples of women who did not find that pregnancy caused weight gain. If you were a bean pole before pregnancy (120 and 5'7) odds are good you are not going to ever become obese, no matter what you do. You do not have the genetics for obesity.

I don't understand why people cannot understand what I am trying to say. If you are a female who has the genetics for obesity, progesterone is yet another factor that can contribute to weight gain. If you are entirely obesity resistant, this probably does not apply to you.

Out of 1000 women who take depo-provera (a synthetic progesterone depot injection), you find a signficant number of those women develops body fat gain, obesity, glucose tolerance disorders and diabetes, PCOS, depression, just as one might expect from natural progesterone.

The fact that 10 women take depot provera and lose weight, have their mood improve, and reduce blood sugars does not negate the trend that women on average taking depot-provera find it causes weight gain, diabetes/sugar disorders, PCOS and depression.

Rereading my post where I spoke of progesterone, pregnancy, and obesity I can see how readers got the idea I was saying that pregnancy ALWAYS causes weight gain. I poorly chose my words and the way I wrote suggested that I was saying progesterone and childbirth always cause obesity or body fat gain.

I did not mean to suggest this as there are obviously many examples of women who have had children, who were thin before, and are thin after. Thin people can not develop obesity if they are not genetically predisposed to it.

It's the "fat" people - the people at risk for obesity for whatever genetic reason - who tend to be affected by factors which trigger obesity, including but not limited to, very elevated progesterone.

Wrong again, Wooo. I'm african-american, with plenty of fat and slim female relatives who are mothers, and the weight gain among the fat ones is simply not 'genetic'. The women who gained after pregnancy reduced activity and increased intake, every single time. There was nothing genetic about their weight gains.

My larger point is that out of a pool of several dozen african-american mothers, the ones who are obese or overweight post-pregnancy are also the only ones who reduced physical activity after each kid while increasing food intake. Also, relatively little breastfeeding. Breastfeeding (not bottle-feeding breast milk, but feeding from the breast primarily for the first year) is extremely protective.

I've never been pregnant or had kids, but paleo2.0 does seem to have a point regarding age of pregnancy and difficulties with weight. Of course there will always be exceptions either way, but my friends who got pregnant in their 20's "bounced back" rather easily compared to those in their early 30's and come those nearing 40 and beyond the struggles post partum were greater no matter never having issues prior.

Interesting bentley that you could not gain weight before pregnancy...but now presumably you can gain weight after pregnancy. Do you not see this as evidence that perhaps pregnancy helps the body to store fat and remain fat?

Not remotely. If the other factors had remained unchanged then I would be more amenable to that possibility but all of the evidence I have experienced personally suggests that the closer I am to the conditions surrounding my prepreg physique the more my post preg physique resembles it.

Nothing short of surgical intervention can erradicate ALL evidence of having been pregnant but this can hardly be compared with the catastrophic level of metabolic derangement being suggested.

"The women who gained after pregnancy reduced activity and increased intake, every single time. There was nothing genetic about their weight gains."

When one begins to develop obesity, the metabolic, endocrine, CNS, nervous system changes result in increased food intake and decreased activity.

You are talking to someone who has been the gamut of weights. I'm 5'5. I've been 280 pounds, I've been 104 pounds. I've seen every extreme of energy mood and hunger. When one is developing obesity, you are constantly hungry and constantly tired. All the food you eat is being shunted into your body fat, it does not give you a feeling of fullness or energy. EVER.

Observing that fat people eat more and move less therefore it is not "genetic" is like saying people with cancer grow too many cells, therefore risk for cancer is not "genetic" either. All they need to do is use willpower to control how often their cells divide, boom no more cancer.

I think youth protects against pregnancy induced obesity only because most humans do not become glucose intolerant until they are in their 30s.

If you are 23, you may have excellent glucose tolerance at this time, therefore at this time you are resistant to a number of obesigenic triggers (e.g. high carbs, high calories, high progesterone levels).

If you are 33, your mitochondria are not as resilient, you are somewhat glucose intolerant, and so those same obesigenic triggers you were resistant to at 23, now they trigger the disease of obesity and diabetes. When you try to eat the pepsis and cookies you could run for days on when you were 23 you feel sluggish, beat, and ravenous, and you gain visible body fat. When you get pregnant at 33, your debilitated glucose metabolism cannot handle supraphysiologic progesterone, which leads to significant glucose intolerance, hyperinsulinemia, gestational diabetes, growth of new fat tissue permanently raising body fat set point.

That is a good point... the fact most people's glucose intolerance onsets later in life may be the reason so many women have adverse pregnancies. Women today wait until 30s to have children.

I wonder if the problem with gestational diabetes may also be related to women delaying pregnancy. If you are almost middle aged when having children, with impared glucose tolerance already, that extra stress of progesterone will push you into diabetes.

I am curious why the readers of this blog have such a problem with the suggestion that progesterone triggers obesity.

This really isn't controversial. Progesterone is well understood by science to cause glucose intolerance, high insulin levels, metabolic abnormalities promoting fetal growth... however, in the context of modern america and obesity, this also promotes obesity and diabetes.

Have you heard of gestational diabetes? You do know that progesterone is the major reason this develops, right?

Or do you superstitiously assume that pregnant women are lazy therefore eat too much, therefore become both fat and diabetic?

OBJECTIVE—Progesterone has a known diabetogenic effect. We sought to determine whether the incidence of gestational diabetes mellitus (GDM) is altered in women receiving weekly 17α-hydroxyprogesterone caproate (17P) prophylaxis for the prevention of recurrent preterm birth.

CONCLUSIONS—The use of 17P for the prevention of recurrent preterm delivery is associated with an increased risk of developing GDM. Early GDM screening is appropriate for women receiving 17P prophylaxis.

Gestational diabetes is prone to false positives. The reasons are varied, but it's not as cut and dried as people think.

The women who gained weight post-pregnancy chose to move less and eat more, which is not 'superstition'. It was what they chose to do. Other women chose otherwise, and didn't have problems with weight gain.

Also, women who have disorder that creates recurring preterm delivery are not representative of genpop, so they don't really go to your views.

Certainly pregnancy can alter body composition, that is definitely a real thing that happens, but the act of becoming pregnant is not itself an obesogenic event, as you seem to frame it.

There is a medicine called megastrol acetate. Guess what megastrol acetate Does! It's an appetite stimulant, fat growth promoter given to cancer patients and others with cachexia (medical term meaning loss of appetite due to diseases).Guess what megastrol acetate is!It's progesterone!

Just got off shift from work. One of my patients is an elderly cute confused irish man with a history of lung cancer. Due to his motherly wife's request, we have jacked his megace up to QID (the average dose is BID). This poor guy can't stop eating and is blowing up like a balloon, all fat. I think I am going to have to convince the doctor and wife that no man should be asking for food every hour and complaining that his clothes no longer fit. She's one of those old fashioned women who thinks eating a lot and being fat is good.

Another fun fact about both megace as well as progesterone: these are substrate for cortisol, the body converts it into glucocorticoids. This helps with pregnancy by ramping up cortisol levels (which then helps prevent fetal rejection and promotes more glucose release).

Megace must be tapered down for this reason as it causes adrenal suppression. Abruptly stopping megace, as well as high dose progesterone, can cause addisonian crisis.

Like I said, paleo2.0... progesterone absolutely causes weight gain and metabolic abnormalities consistent with obesity and diabetes. The fact YOU personally are resistant to this, and the fact SOME women are resistant to it, does not obliterate the trend, and the trend is that women get fat and diabetic after pregnancy, some tremendously so, presumably these are the women who already have pro-obese and diabetic factors going on.

NO woman man or child CHOOSES to eat more and move less. That is superstition.

When I was on leptin I ate like, 1600 calories per day. I also moved a LOT and had energy for days.

Now I eat , like, 2000 calories or more per day. I move far less and don't have the energy I used to.

I did not make a "CHOICE" to do these things. My body changed, and so I move less and eat more. The fact you can not relate to these events because you are obesity resistant does not mean they aren't real.

The reason progesterone is so popular for cachexic patients is a few reasons.

1) It is not a fancy drug; it's dirt cheap, medicare pays for it. It's just basic progesterone in a sippy cup.

2) It works. Give the megace, suddenly people are hungry and getting fat.

3) It's antineoplastic. Megace is very good for cancer because as a progestin, it helps bolster cortisol levels which slows anabolic activities in the body. Most cancer patients are placed on dexamethasone anyway to slow cell growth... adding in megace is just like, an extra helping hand.

4) It's well understood. It's progesterone. We know what progesterone does. It's a naturally occurring female sex steroid. You're not going to get weirdo side effects or drug-drug interactions you didn't anticipate. It doesn't have the drug regulation problems of cannabis derivatives either.

I find it beyond ironic that retarded altie quacks on the interweb convince women that buying progesterone creams from them will make them slim and trim, meanwhile doctors and nurses all over the country are fattening sick dying people up with progesterone. That's a lolz.

Most women do not get fat and diabetic after bearing and nursing children. That is where you are wrong. It is NOT the norm to have the behaviors you're describing. My experience and those of the other mothers posting to this thread is the historical and biological norm.

Certainly NEAT varies from person to person, but near-total cessation of physical activity and mindless eating without hunger cues are usually choices. The women I've seen get fat weren't screaming of hunger as you've reported is your experience. They just sat around nibbling and nibbling their way to fat gain. A choice.

Your fat gain is anomalous and atypical, and that's cool, it's good to hear about unusual cases. But extrapolating from there is, well, inaccurate.

See paleo, this is where you are WRONG. If you ask a crowd of mothers "hey ladies, do you find you are equally as thin after having children" the MAJORITY of these mothers are going to say "no way jose" AND I KNOW THIS because I live in the real world with real people and permanent weight gain after pregnancy is one of the most common complains obese women have.

This is also why non-obese people say stuff like "insulin doesn't make you hungry, it just makes you full" and "carbs have nothing to do with obesity, that atkins/taubes/etal was a quack". I know they are full of crap and have no idea what they are talking about. They read a study here or there, lack a critical understanding of the big picture, and then go around telling people totally false information. Not maliciously, but because of inadequate understanding of obesity informing their half cocked ideas.

And again, re: your fat family...

Gee paleo2.0 it's awesome that you make the choice to be less hungry and to feel more energetic than your fat family members.

Can you teach me that trick? I sure do miss the way I felt on leptin, with rocket energy all the time and dancing off any food I ate, and my fat cells pouring out fatty acids leading to my body fat SPECFICIALLY being lost. How can I choose to have this occur again? Teach me yer secretz! I hate to crap the way I feel now off of leptin but if you can show me the light so I can learn how to choose to feel energetic and move a lot again, and learn not to always be so hungry that I eat 2500 calories per day anymore, I would gladly adopt this new knowledge.

I miss my toothpick arms! Can I has them back?I liked looking like a model, may I has it back?

I mean, I'm still skinny/thin/etc... but I sure would like to not gain any more weight AT ALL, so if you could teach me your trickz that allowed you not to be a fat lazy slob like your family members, I'd be so appreciative.

Wooo, let's just agree to disagree on the set of 'all mothers' and whether a majority of them are 'fat and diabetic' after childbearing and nursing.

I am just another mother, easily tired after a day of playing with my extremely active infant. I get just as tired as my fat female relatives did when their kids were little. But where they sit around and sat around eating when tired, I sit and don't eat. And then I get up and do some moving around anyway.

I am tired right now, but I'm probably going to spend ten minutes before bed picking up my 25lb infant and tossing her in the air. I'll probably also do a few pull-ups.

Like I said, NEAT varies from person to person, but we can all decide consciously to eat less or move more by some non-trivial amount. I don't begrudge people not wanting to do that, but just like you are slim due in no small part to your conscious choices, so are others larger and fatter due to theirs.

We all pick what we can live with, really.

I used to be like you and believed that having children would leave me fat and sick. No, I still have sixpack abs and weigh less than before the baby. I guess I'd suggest you get pregnant and nurse on demand for at least six months. Seems to work pretty well for most women who choose to do so.

For those who want to better understand the challenges faced by the obese and their helpers, consider the fine blogs by Arya Sharma, drsharma.ca , and Yoni Freedhof, bmimedical.com . These doctors work with the obese to help them lose weight, and I am impressed with their compassion and toughness, too. This particular piece gives an insight into the kinds of things they offer on their blogs, and it addresses some of the issues discussed here in the last week:

All amounts of progesterone work to cause an increase in fat storage, eating, and a decrease in thinking/movement.

The higher the progesterone, the worse the trend.

There is no level of "progesterone" where one has better glucose tolerance, better energy, and loses body fat from it. Progesterone cream sheisters on the interwebz lead women to believe that using their product will give energy , improve glucose tolerance, lead to lower appetite and fat loss. This is counter to reality.

Just like thyroid hormone exists in a dose dependent fashion with metabolic activity - meaning to say ALL amounts of T3 will lead to more metabolic activity; there is never a level of T3 where metabolic activity slows down - so it is with progesterone. As soon as it hits those receptor(s) it does what it does and the body shifts to not using glucose well, storing fat, increasing hunger, decreasing swiftness of thought and energy and mood.

Hyperthyroidism is to pregnancy what euthryoid is to almost no progesterone. That means to say, the "normal state" is nearly NO progesterone, much like the "normal state" of thyroid is euthyroidism, just enough T3 to keep your body working properly without symptoms of hyperanabolism.

The normal state for non-pregnant or non-potentially pregnant human beings is almot undetectable levels of progesterone - only people with rare endocrinopathies have progesterone higher than this.

It is a complete, total, 100% myth that any level of progesterone leads to energy/glucose tolerance/weight loss. The more progesterone, the more your body is shifting toward diabetes and weight gain. This is because progesterone only has a role for supporting pregnancy and is only of use to pregnant or potentially pregnant females. That progesterone does much of anything else is pure, altie internet quack fantasy... and I repeat, the goal is to sell you suckers progesterone cream or pills.

Yes, it is true that progesterone does have OTHER roles in the body besides supporting pregnancy, however, the very trivial amounts synthesized by the adrenal glands will cover that just nicely. The only people who need to supplement progesterone, are females who are taking estrogen, and the only reason to do this is to prevent cancer (as progesterone helps suppress estrogen signaling and will prevent some types of estrogen mediated cancers).

All progesterone signaling is pushing the body toward eating, gaining weight, and high glucose, specifically for nurturing a fetus. This is why women and men have negligible progesterone levels, and the only people who have high progesterone are women who have just ovulated (therefore may be pregnant), and women who definitely ARE pregnant. These are the only people who NEED progesterone: pregnant or potentially pregnant women.

Now, it is true that MOST women will not become diabetic or obese from it. However, if you already have an underlying metabolic disorder, monthly progesterone is another aggravating factor for weight gain and blood sugar control. And,if you have poor glucose tolerance at baseline, progesterone is a HUGE trigger for causing profound obesity and diabetes... which is why so many chubby women who have always gotten shaky an hour after eating suddenly find after their first child they are now very obese women with gestational diabetes.

A lot of hormone names are misnomers; the initially understood function later turns out to be incorrect with further research. For example, the original name of the increntin hormone was "orexin" as it was observed to increase appetite in animals. Later it was discovered that incretin actually is responsible for wakefulness, energizing the brain and body and increasing metabolism... the increased eating is merely a result of increased metabolic activity, and a lack of it actually leads to obesity.

"Leptin" was named this way as well. Leptin is derrived from the greek word for thin, leptos, as leptin was originally believed to make animals thin. Now we understand that leptin only regulates the anti-starvation response of the body, it does not cause thinness outside of this.It only causes thinness in animals who do not have leptin signaling due to abnormal lack of leptin. This is an extremely infintismally rare form of obesity - garden variety obese people have relatively normal leptin binding, they are obese for other reasons.

When "serotonin" was discovered it was believed to primary influence the vascular system (sero-tonin) . Only later was its effects on the stress response in the brain, anxiety and mood understood... this is now its better known funciton.

But that's a tangent.

Anyway, "progesterone" is one time where the scientists got it right straight away. Pro, gestational, hormone. Thats what it does, that's why it exists. I guess if you want to err your physiology toward pregnancy (fattening lethargy sleepiness, poor blood sugar control, etc) then go head and dose up.

Not to be too repetitive, but my mom spent 5 years either pregnant or breast feeding (really, no break) and had the last of us (4 kids) at age 30. She gained tons of weight with each pregnancy (50 lbs-ish) but went back to a skinny 125 lb. (she's tall) every time, the weight of her teens.

I am puzzled by the idea of obesity as an inborn disease. Of us four siblings, two are slim and two are overweight. The two overweight have very different body types: one was more athletic, the other a skinny-minny, like my mom. Us slim ones have remained slim, but are athletically built. Point-being, we are all genetically-related as sisters, but have different levels of leanness as adults. And even among the fat, those two have little in common, as the outside would see it. Their problem is that both like processed food: one the junky kind including fast food, the other "healthy" but high-reward rich foods and many years of vegetarianism, including vegan "meats" etc. And, to be honest, she just has a big appetite. Anyway, its a fork to mouth problem and a food choice problem. We all grew up eating the same stuff and we were all lean to skinny as kids: it was adulthood--and the diverging diets--that made us have different levels of leanness.

Hey, maybe APPETITE IS BIOLOGICAL and it isn't a "fork to mouth" problem?

Why is it 2 days after ovulation I have a massive "fork to mouth" problem , and then it magically gets better and I become a good clean moral person who easily burns fat and uses glucose for energy 2 days before menses?

Science (that devil's invention) leads me to believe the cause is progesterone induced glucose intolerance + hyperinsulinemia. However, I have already been told by the internet experts here that progesterone does not cause glucose intolerance or high insulin levels (and I have been told by experts previously that high insulin only leads to satiety). Does my morality shift with my hormone status? Maybe those guys who said women were evil/dirty were right. KEY TO NOT BEING FAT: Don't be an evil woman.\

Why is it that my rather severe "fork to mouth" problem was critical when I was a teenager, before I discovered glucose intolerance and a low carbohydrate diet? Why did my "Fork to mouth" problem magically get better the minute my body saw ketones and the insulin levels dropped?

It's amazing how our morals and choices seem to absolutely correlate with physiology.

It almost suggests that none of this is a choice at all... that it is the result of physiology.

That sounds like some crap crazy Taubes or Atkins would say, so scrap it.

Fork to mouth problem, got it.

Need to choose to be a better person, check.

The stupidity of people regarding the innateness of obesity makes me sick ...until I remember that there are way more tragic things in the world to care about than people being prejuded against fat.

PS, you are not a clone of your siblings. It is entirely possible, although very unlikely, that you and your sister don't even have ONE GENE in common. Most siblings have quite a few genes in common, but some have more than others. This is why two sisters can be clones, but the third looks like an alien compared to them.

The fact two of you are fat and two of you are thin suggests you have very different metabolic traits.

Hey, I was a 300 pound fatty and this is absolutely genetic, I can trace it down my family tree, the glucose intolerance genes, right back to my maternal great grandmother. I have the same skull shape and body composition as my mother, who has it like her mother, who was a north african heralded from a tribe. I mean, I see all of my grandparents in my appearance, but clearly I take the most after her.

My brother has a body type exactly like my maternal great grandfather. Same skull shape, very anglo-saxon/german looking, same height, same body type. Slightly muscled, does not accumulate fat, resists weight gain, good glucose tolerance. He is obesity resistant. He is an almost exact clone of my grandfather, it's sort of scary.

I remember being 16 years old and standing at the statue of liberty with my parents. This is well before I knew anything about obesity other than the fact I was very fat.

I will never forget watching parents and children from all over the country, all ethnicities, standing together. Watching these pairs of adults and children one thing became obvious - obesity was genetic.

The thin children typically had thin parents; the fat children almost always had fat parents.

But waht was especially interesting was how the body shape was the same. A child with squat legs and a bulbous belly was always situated next to a parent with squat legs and a bulbous belly. A gangly child with long legs and arms was seen next to a gangly adult with long arms and legs. The shape of every body part was identical; the overall form of each human being - including how much and where fat was distributed - was clearly genetic.

Seeing all these people in the exact same environment with very different bodies made it so obvious. Like watching tigers + cubs and bears + cubs and wolves + pups all wandering about in a zoo... instantly you realize that the difference between tigers, bears, and wolves is genes. They are all in the same zoo, same environment, but one looks like a tiger, one looks like a bear, one is a wolf. GENES.

Then here I am, 250ish pounds next to my mother, I am her clone, and she is 250ish pounds.

Then you turn to my brother, who looks like a living picture of my dead grandfather. Right down to his weight and height. He even has nervous tics just like he did (he tends to stick his toungue in his cheek, just like my grandfather did - my brother NEVER met him, the tendency for this behavior is clearly genetic).

"Plain, repetitive starchy foods do not lead to fat gain and can support fat loss."

Was that not exactly what they were stuffing themselves with ("mostly sorghum") to gain all that weight in the first place? Some confirmation bias in play, perhaps. ;)_____________Confirmation bias, YES ... MASSIVEly so

About Me

I'm a writer and science consultant with a background in neuroscience and obesity research. I have a BS in biochemistry and a PhD in neurobiology. I'm the author of "The Hungry Brain: Outsmarting the Instincts That Make Us Overeat".

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This blog is a compilation of my opinions. It's not advice; it's information that you can take or leave as you please. I don't intend it to replace professional medical consultation or treatment. Your health is in your own hands.